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Ageing and endothelial progenitor cellrelease of proangiogenic cytokines

机译:促血管生成细胞因子的衰老和内皮祖细胞释放

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SIR—Circulating endothelial progenitor cells (EPCs) arenwidely recognised to contribute to the reparative process ofnResearch lettersn268nDownloaded from ageing.oxfordjournals.org at Institute of Scientific &Technical Info of China on July 21, 2011nthe vascular endothelium and participate in angiogenesis [1].nAlthough declines in the circulating population of EPCs arenassociated with poor cardiovascular disease prognosis and arenpredictive of future adverse cardiovascular events [2], transplantationnof ex vivo expanded EPCs into the coronary arteryncan rescue ischaemic tissue and significantly improve coronarynfunction in patients with myocardial infarction [3]. Thenangiogenic potential of these cells can be explained, in part,nthrough their ability to home to local sites of ischaemia andnvascular damage and secrete potent proangiogenic factors,nsuch as cytokines, chemokines and growth factors, whichnare integral in promoting new blood vessel formation and repair.nFor example, both vascular endothelial growth factorn(VEGF) [4] and granulocyte-colony stimulating factor (GCSF)n[5] stimulate recruitment and migration of EPCs fromnthe bone marrow, inhibit apoptosis and support the angiogenicncapacity of mature endothelial cells [6, 7]. In addition,ninterleukin (IL)-8, a proangiogenic cytokine, has been shownnto attract EPCs to infarcted tissue and enhance the effect ofnG-CSF to mobilise progenitor cells from the bone marrown[8–10]. In older adults, endothelial injury and compromisednEPC-mediated vascular repair are thought to contribute tonatherosclerosis [11]. We have previously reported that EPCncolony-forming capacity, migration and telomere length declinenwith ageing [12, 13]. In the present study, we testednthe hypothesis that the capacity of circulating EPCs to releasenproangiogenic cytokines declines with age in healthy adults.
机译:SIR-循环内皮祖细胞(EPC)有助于nRe研究字母n268n的修复过程。n科研文献n268n从2011年7月21日从ageing.oxfordjournals.org下载。n血管内皮并参与血管生成[1]。在与心血管疾病预后差,未来不良心血管事件无关联的循环EPC中[2],离体移植EPC将扩张的EPC植入冠状动脉冠状动脉抢救性缺血组织中,并显着改善心肌梗死患者的冠状动脉功能[3]。这些细胞的血管生成潜力可以部分地通过其对局部缺血和血管损伤的部位的归巢能力以及分泌有效的促血管生成因子(如细胞因子,趋化因子和生长因子)的能力来解释,这些因子在促进新血管的形成和修复中是不可或缺的。 n例如,血管内皮生长因子(VEGF)[4]和粒细胞集落刺激因子(GCSF)n [5]都刺激EPC从骨髓募集和迁移,抑制细胞凋亡并支持成熟内皮细胞的血管生成能力[6, 7]。此外,已显示促血管生成细胞因子白介素(IL)-8可以吸引EPC到梗塞的组织中,并增强nG-CSF从骨髓中动员祖细胞的作用[8-10]。在老年人中,内皮损伤和dnEPC介导的血管修复受损被认为是导致动脉粥样硬化的原因[11]。我们以前曾报道过,随着年龄的增长,EPC菌落形成能力,迁移和端粒长度下降[12,13]。在本研究中,我们检验了健康成人中循环EPC释放促血管生成细胞因子的能力随年龄下降的假说。

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